Bispecific T-cell engager antibody that binds CD19 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and redirect endogenous T cells to kill CD19-positive malignant B cells.
Bispecific antibody that simultaneously binds CD19 on B cells and CD3 on T cells, forming an immune synapse to activate TCR/CD3 signaling and redirect endogenous T cells to kill CD19-positive malignant B cells; includes an albumin-binding domain to extend half-life.
Bispecific antibody bridges CD19 on target cells to CD3 on T cells, forming an immune synapse that activates T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity.
Anti-HER2 antibody–drug conjugate that binds HER2, is internalized, and releases MMAE to inhibit microtubules, causing cell-cycle arrest/apoptosis and potential ADCC.
Anti-HER2 antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis; may also mediate Fc-dependent ADCC.
Binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
Autologous CD19-directed CAR T-cell therapy (Breyanzi) composed of defined CD4+ and CD8+ T cells engineered to express an anti-CD19 CAR, targeting and killing CD19+ B cells.
Autologous CD4+ and CD8+ T cells are engineered with a lentiviral vector to express an anti‑CD19 chimeric antigen receptor containing 4‑1BB costimulatory and CD3ζ signaling domains. Upon binding CD19 on B cells, the CAR activates T‑cell effector functions, leading to proliferation, cytokine release, and targeted lysis of CD19+ malignant B cells. A truncated EGFR tag enables in vivo tracking and potential elimination of the modified cells.
Anti-CD19 CAR T cells recognize CD19 on B cells, become activated (4-1BB/CD3zeta signaling), and kill targets via T-cell cytotoxicity (perforin/granzyme and Fas-FasL).
Bispecific T‑cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on target cells to activate T‑cell cytotoxicity, including against CF33‑CD19–tagged tumors.
Bispecific CD3xCD19 T-cell engager (BiTE) that links T cells to CD19-expressing target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme) to kill CD19+ cells; in this trial, redirects T cells to CF33-CD19-tagged tumors.
Blinatumomab bridges CD3 on T cells to CD19 on target cells, forming an immune synapse; engaged T cells kill CD19+ cells via perforin/granzyme-mediated cytotoxicity (apoptosis/lysis).
A humanized anti-CD20 monoclonal antibody (biologic) administered by IV infusion that depletes CD20+ B cells via ADCC, CDC, and apoptosis; used to reduce B-cell–mediated immune activity in multiple sclerosis.
Humanized anti-CD20 monoclonal antibody that binds CD20 on pre-B to mature B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis, reducing B cell–mediated immune activity (e.g., antigen presentation and proinflammatory cytokine signaling) in multiple sclerosis.
Ocrelizumab binds CD20 on B cells and depletes them via Fc-mediated ADCC, complement-dependent cytotoxicity, and induction of apoptosis.